Method and device for treating dysfunctional cardiac tissue

ABSTRACT

Various methods and devices are provided for reducing the volume of the ventricles of the heart. In one embodiment, a method for reducing the ventricular volume of a heart chamber is provided including the steps of inserting an anchoring mechanism onto dysfunctional cardiac tissue, deploying one or more anchors into the dysfunctional cardiac tissue, raising the dysfunctional cardiac tissue using the anchors, and securing the anchors to hold the dysfunctional cardiac tissue in place. Further, a device for reducing the volume of the ventricles of a heart chamber is provided where the device has one or more clips for placement on dysfunctional cardiac tissue of a heart, one or more anchors for deployment and securement into the dysfunctional cardiac tissue, and a lifting mechanism for raising the one or more anchors and the dysfunctional cardiac tissue.

This application is a continuation of U.S. patent application Ser. No.13/966,049 filed on Aug. 13, 2013, which is a divisional of U.S. patentapplication Ser. No. 11/507,146 filed on Aug. 21, 2006, which claims thebenefit of provisional patent applications Ser. No. 60/709,730 filed onAug. 19, 2005, Ser. No. 60/709,690 filed on Aug. 19, 2005 and Ser. No.60/711,727 filed on Aug. 26, 2005.

BACKGROUND OF THE INVENTION

Field of the Invention

This invention relates generally to devices for resizing ventricle andrelated methods for placing the devices. More particularly, it relatesto sizing devices for reducing the ventricular volume to improve theheart's pumping action. The devices and methods of the present inventionare directed toward thoracoscopy or subxiphoid techniques used tofacilitate sizing of the ventricles.

Prior Art

Heart failure (HF), the heart's inability to pump an adequate volume ofblood to the tissues, is the only major cardiovascular condition thatcontinues to increase in incidence in the United States. Approximate 5million patients are currently diagnosed with HF in the United States.The American Heart Association estimates that 550,000 new HF casesdevelop each year. This condition is responsible for an estimated900,000 hospitalizations annually—more than any other medical conditionamong the elderly. Approximately 6.5 million hospital days each year areattributed to and related to HF and as many as one third of thosepatients are readmitted for treatment of symptom recurrence within 90days. Thus, it is not surprising that the cost of providing advancedmedical care for the millions of patients suffering from HF isextraordinarily high—now estimated at more than $38 billion annually.

In certain pathological conditions, the ventricles of the heart becomeineffective in pumping the blood, causing a back-up of pressure in thevascular system behind the ventricle. The reduced effectiveness of theheart is usually due to an enlargement of the heart. Coronary arterydisease causes approximately 60% of congestive heart failure. Acutemyocardial infarction (AMI) due to obstruction of a coronary artery is acommon initiating event that can lead ultimately to heart failure. Amyocardial ischemia may, for example, cause a portion of a myocardium ofthe heart to lose its ability to contract. Prolonged ischemia can leadto infarction of a portion of the myocardium (heart muscle) wherein theheart muscle dies and become scar tissue. Once this tissue dies, it nolonger functions as a muscle and cannot contribute to the pumping actionof the heart. When the heart tissue is no longer pumping effectively,that portion of the myocardium is said to be hypokinetic, meaning thatit is less contractile than the uncompromised myocardial tissue. As thissituation worsens, the local area of compromised myocardiwn may in factbulge out as the heart contracts, further decreasing the hearts abilityto move blood forward. When local wall motion moves in this way it issaid to be dyskinetic. The dyskinetic portion of the myocardium maystretch and eventually form an aneurysmic bulge.

One problem with a large dilated left ventricle is that there is asignificant increase in wall tension and/or stress both during diastolicfilling and swing systolic contraction. In a normal heart, theadaptation of muscle hypertrophy (thickening) and ventricular dilatationmaintain a fairly constant wall tension for systolic contraction.However, in a failing heart, the ongoing dilatation is greater than thehypertrophy and the result is a rising wall tension requirement forsystolic contraction. This is felt to be an ongoing insult to the musclemyocyte resulting in further muscle damage. In response, the hearttissue remodels to accommodate the chronically increased tillingpressures, further increasing the work that the now-compromisedmyocardium must perform. This vicious cycle of cardiac failure resultsin the symptoms of congestive heart failure such as shortness of breathon exertion, edema in the periphery, nocturnal dypsnia (a characteristicshortness of breath that occurs at night after going to bed), weightgain, and fatigue, to name a few. The increase in wall stress alsooccurs during diastolic filling. The stress increase requires a largeramong of oxygen supply, which can result in exhaustion of the myocardiumleading to a reduced cardiac output of the heart.

The incidence of ischemic dilated cardiomyopathy is increasing, not onlyas a consequence of the aging of the population, but also becauseeffective emergency interventions for otherwise fatal acute coronaryevents are extending the lives of many patients with ischemic congestiveheart failure (CHF). Despite the major advances in both medical andsurgical therapy, the management of patients with coronary arterydisease and left ventricular (LV) dysfunction continues to bechallenging due to the complex and multifactorial pathophysiology ofthis condition.

Since heart transplantation, when indicated, continues to be limited byseveral factors, conventional surgical treatment for ischemiccardiomyopathy has gained increasing attention in recent years and avariety of therapeutic interventions have been developed or optimized.

It has been demonstrated that myocardial revascularization and valverepair are capable of improving left ventricular function.

Recent efforts have concentrated on improving left ventricular functionby means of surgical methods aimed at ventriculoplasty with or without areduction in ventricular volume.

Prior treatments for heart failure associated with such dilatation fallinto three general categories. The first being pharmacologicaltreatment, for example, diuretics and ACE inhibitors, The second beingassist devices, for example, pumps. Finally, effective surgicaltreatments also have been performed with, for example, Dor or Jateneprocedure, or left ventricular reconstruction (LVR), which requires theuse of cardiopulmonary bypass (CPB) machine.

Many patients who would benefit from left ventricular reconstruction arethe least likely to withstand the effects of CPB due to age, poorejection fraction, or other cardiovascular disease. Therefore, thereremains a need for an efficient device and method for reducingventricular volume.

SUMMARY OF THE INVENTION

This invention relates to a device and method for completely off-pumptreatment of congestive heart failure patients, and particularly, asizing device and method for excluding infarcted tissue and reducingventricular volume. The device and method may be performed minimallyinvasively which is less traumatic to the patient than an open-chest andopen-heart surgical technique.

Thus, a more recent technique for treating the various forms of heartfailure discussed above includes placing devices on the heart to excludeinfarcted tissue and to reduce the ventricular volume. The devices areconfigured to reduce the ventricular volume, hence to reduce the tensionin the heart wall, and thereby reverse the disease process of a failingheart.

An aspect of the present invention pertains to a clip or clamp device,and related clip methods, for thoracoscopic device placement on theheart. The clips of the present invention may be placedthoracoscopically. The inventive techniques and devices thus areminimally invasive and less risky to patients.

According to an aspect of the invention, a method for placing the clipassembly anterior a heart chamber around the infarcted tissue comprisesproviding a flexible and strong member having a clip or clamp and adeployable anchoring assembly connected to at least one end. The methodfurther includes advancing an anchoring member through vasculaturestructure and into the heart chamber such that the first end of theanchoring member extends through infracted tissue of a wall through theheart chamber wall and pull the infarcted tissue into or around the clipor clamp to exclude the dysfunctional tissue to reduce ventricularvolume.

Yet another aspect of the invention includes a delivery tool fordelivering a transventricular volume reduction device to chamber of theheart, comprising a tubular member having a distal end and proximal end,the distal end having an anchoring element and the tube defining a lumenor suture configured to carry at least a portion of the anchoringassembly. The delivery tool further includes at least one supportmechanism disposed proximate the distal end of the tubular member, thesupport mechanism being configured to stabilize the tubular member withrespect to a heart wall surrounding the chamber. The tubular member isconfigured to be advanced through vasculature structure and into theheart chamber.

In view of the above need for treating the dysfunctional tissue, thepresent invention provides a system and method incorporated into theclip or clamp device and employs small quantities of drug to beadministered over an extended period of time to the heart tissues. Themethods of the present invention thus avoid the pitfalls associated withsystemic delivery of a drug.

A further advantage of the present invention is that it avoids problemsassociated with bolus injection of a drug, such as delivery of an amountof drug to the cardiac tissue, which is too high and which therefore mayhave deleterious effects on the cardiac tissue.

Another advantage is that it provides long-term delivery of a drug tothe pericardium or myocardial tissue, with even delivery rate.

Still another important advantage is that extended delivery of a drug tothe cardiac tissue can be achieved during the placement of clip or clampfor dysfunctional tissue exclusion, without the need for invasivesurgery, thereby reducing trauma to the patient.

Further, in view of the above need of treating the dysfunctional tissue,the present invention provides a system and method incorporated into theclip or clamp employing transducers/sensors for determining the heartfunction and parameter and measuring heart performance of both left andright ventricles, particularly the left ventricle without requiringinvasive surgery to access the left ventricle.

The sensors comprise at least a first sonomicrometer piezoelectriccrystal mounted on a clip or clamp, so that when clip or clamp isimplanted on the heart chamber, on does the sensor. One or moreadditional sonomicrometer piezoelectric crystals can be mounted on theclip or clamp, such that the distance between the three or moresonomicrometer crystals can be determined. In each case, thesonomicrometer crystal are distributed about a heart chamber of interestsuch that the distance between the separated ultrasound transmitter andreceiver crystal pairs changes with contraction and relaxation of theheart chamber.

The invention thus involves the incorporation of sonomicrometerpiezoelectric crystals into the clip or clamp.

A principal advantage of the system and method of the present inventioninclude the ability to directly monitor left ventricular functionwithout opening the left side of the heart. The system and method of thepresent invention is advantageously employed to measure cardiacdimensions in real time and to either record or transmit these valuesfor monitoring purposes or to use these values as feedback to modify thedelivery of electrical or pharmacological therapy, particularly in thetreatment of heart failure.

The system and method of the present invention can be advantageouslyemployed in the detection of electromechanical association during pacingor arrhythmias, differentiation of hemodynamically significant andinsignificant ventricular tachycardias, monitoring of cardiac output,ventricular volume, determining the need for aggressive and lessaggressive pharmacological therapies, and the like.

The above and other features of the invention, including various noveldetails of construction and combinations of parts, will now be moreparticularly described with reference to the accompanying drawings andpointed out in the claims. It will be understood that the particulardevice embodying the invention is shown by way of illustration only andnot as a limitation of the invention. The principles and features ofthis invention may be employed in various and numerous embodimentswithout departing from the scope of the invention.

BRIEF DESCRIPTION OF THE DRAWINGS

These and other features, aspects, and advantages of the apparatus andmethods of the present invention will become better understood withregard to the following description, appended claims, and accompanyingdrawings where:

FIGS. 1-9 illustrate an anchoring system used for reducing ventricularvolume of a heart in accordance with an embodiment of the presentinvention;

FIGS. 10A-19 illustrate various other embodiments for reducingventricular volume of a heart in accordance with the present invention.

DETAILED DESCRIPTION OF THE INVENTION

Although this invention is applicable to numerous and various types ofcardiovascular methods, it has been found particularly useful in thefield of reducing ventricular volume of the heart. Therefore, withoutlimiting the applicability of the invention to the above, the inventionwill be described in such environment.

With reference to FIGS. 1-9, an anchoring system in accordance with oneembodiment of the present invention will be described.

Initially, in FIG. 1, a subxiphoid incision is cut to create an opening101 to access the ventricles of the heart. Additional access may beperformed in the intercostal space for other instruments as well. Then,a double balloon catheter 102 is introduced into the heart through theopening 101 to unload the heart. The balloon catheter 102 providesinflow occlusion to decompress the ventricles, thereby reducing thesystolic pressure for aid in reducing the ventricular volume orexclusion of dysfunctional cardiac tissue. The catheter 102 can beplaced surgically in an open chest or via femoral or subclavian veinspercutaneously.

As seen in FIG. 2, an anchoring mechanism 100 is then inserted through adelivery tool 120. The delivery tool 120 comprises a tubular memberhaving a distal end and proximal end, the distal end having theanchoring mechanism 100 protruding from it. The tubular member isconfigured to be advanced through vasculature structure and into theheart chamber.

The anchoring mechanism 100 is brought through the delivery tool 120 andthen positioned on an epicardial surface where the dysfunctional cardiactissue 103 is located. The anchoring mechanism 100 can have a flexiblebottom portion 104 with clips 105, 106, and a top portion 108 with oneor more anchors 110. The clip 106 has a bottom surface 106 a having pods107, which can be seen clearly in FIG. 2b , which shows across sectionalview of the clips 105, 106 with pods 107. The pods can be used todeliver hear failure drugs such as bet blocker, ACE, ARB, etc., whichcan be released slowly onto the dysfunctional cardiac tissue 103.

Further, several sonomicrometer crystals sensors (not shown) are locatedon the clips 105, 106 which are implanted in or on the patient's heart.The sensors are used for determining the heart function and parameterand measuring heart performance of both the left and right ventricles.The sensors comprise at least a first sonomicrometer piezoelectriccrystal mounted on the clips 105, so that when the one or more clips 105are implanted on the heart chamber, so does the sensor. One or moreadditional sonomicrometer piezoelectric crystals can be mounted on theclips 105, such that the distance between the sonomicrometer crystalscan be determined. In each case, the sonomicrometer crystal aredistributed about a heart chamber of interest such that the distancebetween the separated ultrasound transmitter and receiver crystal pairschanges with contraction and relaxation of the heart chamber.

Then, as shown in FIG. 3, the anchoring mechanism 100 is inserted in thedysfunctional tissue 103. The top portion 108 is used to insert theanchors 110 through the dysfunctional tissue 103 and into the heartchamber such that a bottom end of the anchors 110 extends through theinfarcted tissue into or around the clips 105. As seen in FIG. 4, theanchors 110 are slowly deployed into the dysfunctional tissue 103. InFIG. 5, anchor deployment is completed and the anchors 110 are lockedinto the dysfunctional tissue 103. The anchors 110 have a bottom endthat deploys such that once it goes through the dysfunctional cardiactissue 103 it opens up to secure itself to the dysfunctional cardiactissue 103.

Then, as shown in FIG. 6, first the central tissue is brought up usinganchor 110 a. Any mechanical means can be used to raise the anchor 110a, such as a screw or clamp which can be operated by a doctor. Theflexible bottom portion 104 of the anchoring mechanism 100 also riseswith the anchors 110. Then, as shown in FIG. 7, the distal tissue isbrought up using anchor 110 b. Finally, proximal tissue 110 c is broughtup using anchor 110 c. For purposes of the illustration, three anchors110 are shown, although one or more can be used in the procedure. Nospecific order of raising the anchors 110 is required, and the anchors110 can be raised in any order, In the preferred embodiment describedabove, the central anchor 110 a is raised first, then the distal anchor110 b, and then the proximal anchor 110 c.

At the completion of the procedure, as shown in FIG. 9, the anchors 110are secured. The anchors 110 can be secured using a screw thread meansor any other means known in the art. The anchors 110 may be secured be azip tag system, where the anchors are pulled together, or the anchors110 can be clamped, or the anchors may even be glued with abio-compatible material. The anchors 110 may, of course, be secured byany other method known in the art and are not limited to the above. Thetop portion 108 is retracted, and the clips 105, 106 and bottom portion104 are left in place with the anchors 110 on the dysfunctional cardiactissue 103 to hold the tissue in place.

The dysfunctional cardiac tissue 103 is now excluded, and the volume ofthe ventricle is reduced to the appropriate volume with the aid oftransesophageal echocardiography (TEE) by controlling the central,proximal and/or distal anchoring mechanism 100. The clips 105 can have acontrolled drug release over an extended period of time.

Various other methods and devices are also possible for reducingventricular volume in accordance with the present invention, which willbe described below with respect to FIGS. 10-19.

FIGS. 10(a)-10(c) illustrate a one way cartridge concept, where a longshaft 202 is connected to an actuator 201 at a distal end and a one-waycartridge at a proximal end. The one-way cartridge comprises a cartridge204 and a suction head 203. The cartridge is connected to the long shaft202 through a remotely detachable joint 206. In practice, the actuatorand long shaft are inserted through a delivery tube to place thecartridge 203, 204 on dysfunctional cardiac tissue 103. The cartridge204 is placed on the dysfunctional cardiac tissue 103, as seen in FIG.10(b), and the suction head 204 lifts up the dysfunctional cardiactissue 103 through the opening 207 of the cartridge 204. The cartridge204 holds the dysfunctional cardiac tissue 103 in place and the suctioncap 203 can be removed.

FIG. 11 shows a variation of the embodiment in FIG. 10, where thecartridge 204 has suction vents 205 along the top of the cartridge 204,and has interlocking parts 204 a and 204 b that make up the cartridge204. Here, after the suction head 203 pulls up the dysfunctional cardiactissue 103, the interlocking parts 204 a and 204 b can be pulledtogether to form a cartridge 204 to secure the dysfunctional cardiactissue 103 in place.

In FIG. 12, another variation of the embodiment above is described,which relies almost entirely on suction to exclude the dysfunctionalcardiac tissue 103. Here, a suction cap/clip is shown having a suctioncap 210, a molded silicon cap 212 and a locking clip 211. The suctioncap/clip assembly is placed on the dysfunctional cardiac tissue 103through a delivery tube, and the molded silicon cap 212 is placed on thedysfunctional cardiac tissue 103. The molded silicon cap issemi-circular in shape, and has slots 213 for the locking clip 211. Thesuction head 210 pulls up the dysfunctional cardiac tissue 103. Themolded silicon cap 212 is then secured and squeezed in to hold thedysfunctional cardiac tissue 103 using locking clip 211 by placing theends of the locking clip 211 through the slots 213. The suction cap 210can then be removed, leaving the molded silicon cap 212 and locking clip211 in place. Materials used for the cap 212 can be silicon or any othermaterial known in the art, such as any bio-compatible material.

FIG. 13 shows another similar embodiment to FIG. 12, where a similar capis placed on top of the dysfunctional cardiac tissue 103. An anchor 221is driven through the cap 220 and through the dysfunctional cardiactissue 103. The end of the anchor 221 has a deployment mechanism whichexpands once deployed through the wall of the dysfunctional cardiactissue 103 to lock into place. The anchor 221 is then pulled up, and thecap 220 bends through forces exerted by the ends 222 and 223. The cap220 can be such that it is under tension from ends 222 and 223, forcingit to compress and bend. Thus, once the anchor 221 is used to raise thedysfunctional cardiac tissue 103 up, the ends 222 and 223 hold the cap220 in place, reducing the ventricular volume.

FIG. 14 shows a similar embodiment which is tightened using a tighteningapparatus 237. First, a cap 230 is placed on top of dysfunctionalcardiac tissue 103 using a tightening apparatus 237. The tighteningapparatus comprises a knob 231, a grip 232, a long shaft 234, and forcetransmitting pins 235. The pins 235 connect to or go through the ends239 of the cap 230. A spring is embedded inside the soft molded outercover of the cap 2230. First the knob 231 is turned to rotate the pins235, which cause the ends 239 of the cap 230 to open up and open the cap230 and place the spring cap 230 under tension, and the cap 230 isplaced on top of the dysfunctional cardiac tissue 103. Then, the knob231 is turned in the other direction to relax spring and bring the cap230 back to its normal position, thus squeezing in the dysfunctionalcardiac tissue 103 between its ends 239. The spring in the cap 230 holdsthe dysfunctional cardiac tissue 103 in place and secures it into thecap 230.

FIG. 15 shows another embodiment where two horizontal pieces 240 a and240 b are placed on top of the dysfunctional cardiac tissue 103, and thedysfunctional cardiac tissue 103 is pulled up using a surgicalinstrument between the pieces 240 a and 240 b. Then, the two pieces 240a and 240 b are pushed together to hold the dysfunctional cardiac tissue103 in place, and secured by any type of locking means known in the art.The two pieces can be screwed together, nailed, tied, or any othermeans,

FIGS. 16-18 show a transventricular anchor system where an anchor isused through a hollow tube to reduce the ventricular volume of theheart.

In FIG. 16, a hollow tube 250 is used to pierce through dysfunctionalcardiac tissue 103, going through the left ventricle 251, through theseptum 253 and into the right ventricle 252 Then, an anchor 257 isdeployed having a long ratcheting member 255 attached to it. One end ofthe anchor 257 is secured inside the right ventricle 252 against thewall of the septum 253. The hollow tube 250 is then removed. A lockingmember 258 is then secured against the ratcheting member 255 and pushedalong the long ratcheting member until it locks into place along thelocks placed alongside the ratcheting member 255. The locking member 258can be pushed as far as required until the ventricular walls of the leftventricle 251 are folded enough to a surgeon's preference. Any excesslength of the ratcheting member 255 can then be cut off and removed.

FIG. 17 shows a preferred variation of the transventricular approachfrom the left ventricle 251. Here, the hollow tube 250 is insertedthrough the left ventricle 251, through the septum 253, and through theright ventricle 252. An anchor 257 is run through the hollow tube andsecured to the outside of the right ventricle 252. The anchor 257 isconnected to a long ratcheting member 255. The hollow tube is thenremoved, and a locking member 258 running along the length of theratcheting member 255 is secured and pushed, locking it into placeagainst the outer wall of the left ventricle, thus reducing the volumeof the left ventricle, as can be seen in FIG. 17.

FIG. 18 shows another variation of the transventricular approach fromthe right ventricle 252. Again, a hollow tube 250 (not shown) isinserted through the right ventricle 252, through the septum 253 andthrough the left ventricle 251 all the way to the outer wall of the leftventricle 251. The hollow tube 250 is removed, leaving the ratchetingmember 255 and anchor 257 behind, similar to the embodiments in FIGS.16-17. The anchor 257 is secured against the outer wall of the rightventricle, and the locking member 258 is pushed along the length of theratcheting member and against the wall of the left ventricle untiltight, thus reducing the volume of the left ventricle, as can be seen inthe figure.

FIG. 19 shows a patch 260 with a deformable slit 261. This device ismade from two components: the deformable slit 261 is formed from fullyannealed stainless steel or other malleable metallic alloy and theattached patch is a woven fabric material, such as the woven fabricmaterial sold under the trademark DACRON. The initial shape of the slit261 has a shape similar to an elongated ellipse. The patch 260 with thedeformable slit 261 is placed on the heart with the center of the slitpreferably 2-3 cm from the LAD and the long axis of the slit generallyparallel to the LAD. The dysfunctional tissue 103 is pulled through theslit using either one or more anchors placed through the tissue 103, orusing the previously described suction device. After the desired amountof tissue 103 has been pulled through the opening, a surgical tool isused to approximate the long edges of the deformable slit 261 to holdthe gathered tissue 103 in place. The effective removal of tissue fromthe ventricular volume and the gathering of the tissue edges togetherreduces the volume and short-axis diameter of the left ventricle as canbe seen from the figure. The gathered tissue 103 is further secured inplace by sewing the cloth material to the epicardial surface of thetissue 103 and by suturing the tissue 103 to the malleable slit 261.

The present invention provides several advantages that solve theproblems with prior art methods. The device and method may be performedminimally invasively which is less traumatic to the patient than anopen-chest and open-heart surgical technique, and reducing the volume ofthe ventricles thus reducing the tension in the heart wall and reversingthe disease process of a failing heart.

Further, the clips/clamps employ small quantities of drug to beadministered over an extended period of time to the heart tissue, thusavoiding the pitfalls associated with systemic delivery of a drug. Thepresent invention avoids problems associated with bolus injection of adrug, such as delivery of an amount of drug to the cardiac tissue, whichis too high and which therefore may have deleterious effects on thecardiac tissue. Another advantage is that it provides long-term deliveryof a drug to the pericardium or myocardial tissue, with even deliveryrate. Extended delivery of the drugs to the cardiac tissue can beachieved during the placement of the clips or clamps, without the needfor invasive surgery, thereby reducing trauma to the patient.

One principal advantage of the system and method of the presentinvention is the ability to directly monitor left ventricular functionwithout opening the left side of the heart. The system and method of thepresent invention is advantageously employed to measure cardiacdimensions in real time and to either record or transmit these valuesfor monitoring purposes or to use these values as feedback to modify thedelivery of electrical or pharmacological therapy, particularly in thetreatment of heart failure. Further, the system and method of thepresent invention can be advantageously employed in the detection ofelectromechanical association during pacing or arrhythmias,differentiation of hemodynamically significant and insignificantventricular tachycardias, monitoring of cardiac output, ventricularvolume, determining the need for aggressive and less aggressivepharmacological therapies, and the like.

The above descriptions of the present invention are specific embodimentsof the present invention and are not limited to the above descriptionsand uses. Various sizes, numbers and types of anchors can be used.Various clips and/or clamps can be used in the anchoring mechanism. Anytype of drugs can be released by the clips/clamps over various times.The anchoring system elements are not limited to what is describedabove, and any type of other anchoring elements can be used to deployanchors into the dysfunctional tissue 103.

While there has been shown and described what is considered to bepreferred embodiments of the invention, it will, of course, beunderstood that various modifications and changes in form or detailcould readily be made without departing from the spirit of theinvention, It is therefore intended that the invention be not limited tothe exact forms described and illustrated, but should be constructed tocover all modifications that may fall within the scope of the appendedclaims.

What is claimed is:
 1. A patch for reducing a volume of a ventricle of aheart chamber comprising: a main body that is positionable aboutdysfunctional tissue of the ventricle, the main body comprising a wovenfabric material; and a deformable slit that extends upward from the mainbody, the deformable slit comprising a malleable metal material, thedeformable slit having a shape of an elongated ellipse and forming acontinuous, closed loop configured to allow the dysfunctional tissue tobe pulled through the loop, wherein: the woven fabric material extendscontinuously around the loop; opposing walls of the deformable slit areconfigured to be displaced inwardly after the dysfunctional tissue ispulled through the loop to secure the patch about the dysfunctionaltissue and reduce the volume of the ventricle; and the opposing walls ofthe deformable slit comprise a more parallel configuration after theopposing walls are displaced inwardly.
 2. The patch of claim 1, whereinthe malleable metal material of the deformable slit is fully annealedstainless steel.
 3. The patch of claim 1, further comprising one or moreanchors that are attachable to the dysfunctional tissue and that areoperable to pull the dysfunctional tissue through the loop of thedeformable slit.
 4. The patch of claim 1, further comprising a suctiondevice that is attachable to the dysfunctional tissue and operable topull the dysfunctional tissue through the loop of the deformable slit.5. The patch of claim 1, wherein the main body extends laterally andoutwardly from longitudinal edges of the deformable slit.
 6. The patchof claim 1, wherein the main body is attached to longitudinal edges ofthe deformable slit.
 7. A patch for reducing a volume of a ventricle ofa heart chamber comprising: a main body that is positionable aboutdysfunctional tissue of the ventricle; and a deformable slit that formsa continuous, closed loop, wherein the loop defines an opening thatallows the dysfunctional tissue to be pulled through the opening,wherein: the main body is attached to the deformable slit and extendscontinuously around an entire periphery of the deformable slit; and theopening of the deformable slit is configured to be reduced after thedysfunctional tissue is pulled therethrough to secure the patch aboutthe dysfunctional tissue and reduce the volume of the ventricle.
 8. Thepatch of claim 7, wherein the main body comprises a woven fabricmaterial.
 9. The patch of claim 7, wherein the deformable slit comprisesa malleable metal material.
 10. The patch of claim 9, wherein themalleable metal material is fully annealed stainless steel.
 11. Thepatch of claim 7, wherein the deformable slit has an initial elongatedellipse shape prior to reduction of the opening and a more parallelconfiguration after reduction of the opening.
 12. A method for reducinga volume of a ventricle of a heart chamber, the method comprising:placing a patch having a deformable slit and an outward flange aroundthe deformable slit onto dysfunctional tissue, wherein the outwardflange is attached to and extends continuously around an entireperiphery of the deformable slit, and wherein the patch forms acontinuous, closed loop; pulling the dysfunctional tissue through thedeformable slit on the patch; and securing the tissue to the deformableslit.
 13. The method of claim 12, further comprising positioning thedeformable slit onto the dysfunctional tissue such that a center of thedeformable slit is within 2-3 cm of a left anterior descending artery(LAD).
 14. The method of claim 13, wherein the deformable slit isfurther positioned onto the dysfunctional tissue so that a long axis ofthe deformable slit is generally parallel to the LAD.
 15. The method ofclaim 12, further comprising pulling the dysfunctional tissue throughthe deformable slit using one or more anchors placed through thedysfunctional tissue.
 16. The method of claim 12, further comprisingpulling the dysfunctional tissue through the deformable slit using asuction device.
 17. The method of claim 12, further comprising reducingan opening of the deformable slit after the dysfunctional tissue hasbeen pulled through the deformable slit to hold the dysfunctional tissuein position, wherein reducing the opening of the deformable slitcomprises moving opposing edges of the opening toward one another. 18.The method of claim 12, further comprising sewing the patch to anepicardial surface of the dysfunctional tissue.
 19. The method of claim18, further comprising suturing the deformable slit to the dysfunctionaltissue pulled through the deformable slit.
 20. The method of claim 12,wherein the outward flange is formed of at least one of a thermoplasticelastomer material or silicone.